Phenomena » Mini-Blogs » Not Exactly Rocket Sciencehttp://phenomena.nationalgeographic.com/blog/not-exactly-rocket-science/
A science salon hosted by National Geographic MagazineTue, 03 Mar 2015 14:31:25 +0000en-UShourly1http://wordpress.org/?v=4.1.1I’ve Got Your Missing Links Right Here (28 February 2015)http://phenomena.nationalgeographic.com/2015/02/28/ive-got-your-missing-links-right-here-28-february-2015/
http://phenomena.nationalgeographic.com/2015/02/28/ive-got-your-missing-links-right-here-28-february-2015/#commentsSat, 28 Feb 2015 21:24:32 +0000http://phenomena.nationalgeographic.com/?p=167116Sign up for The Ed’s Up—a weekly newsletter of my writing plus some of the best stuff from around the Internet.

Top picks

Two boys from either side of the Iron Curtain, united through a love of birds, turn a no man’s land into an ecological success story. This piece from Phil McKenna is one of the best I’ve read recently. I cried at the end.

The time everyone “corrected” the world’s smartest woman, and she was right. A great piece about the Monty Hall Problem.

The Science of Why No One Agrees on the Color of This Dress. Adam Rogers explains.

An Italian surgeon claims that he can do head transplants. It’s complete nonsense. Virtually every new organisation covers it terribly. Azeen Ghorayshi at Buzzfeed does it right.

You think you’re safe and then–BAM–an octopus leaps out of the water and kills you.

Aeon Ideas: the cool topics of Aeon fused with the discussion style of Quora.

“I wanted to tell him that inspiration is a joke and is about as meaningful as a bartender’s smile.”

Comics fan dies of unexplained causes. Family gets obit to list cause of death as “uppercut from Batman”

]]>http://phenomena.nationalgeographic.com/2015/02/28/ive-got-your-missing-links-right-here-28-february-2015/feed/4Fishing For the Microbes Behind Malnutritionhttp://phenomena.nationalgeographic.com/2015/02/25/fishing-for-the-microbes-behind-malnutrition/
http://phenomena.nationalgeographic.com/2015/02/25/fishing-for-the-microbes-behind-malnutrition/#commentsWed, 25 Feb 2015 19:00:42 +0000http://phenomena.nationalgeographic.com/?p=167110Malnutrition seems like an intuitive problem: you don’t eat enough food, so your health suffers. But it’s not that simple. One mysterious type of malnutrition known as kwashiorkor—characterised by leaky blood vessels, puffy limbs, distended stomachs, and fragile skin—often affects children who eat just as much as their healthy neighbours. And even if these kids get to munch on protein-rich food, some don’t recover.

A team of scientists, led by Jeff Gordon at the Washington University School of Medicine, has shown that children with kwashiorkor harbour 11 species of gut bacteria that, together with their poor diets, conspire to damage their guts.

These results suggest that this particular type of malnutrition isn’t just caused by the absence of food, but also by the presence of the wrong microbes.

The team first started studying kwashiorkor in Malawi a few years ago, after noticing that some children developed the condition while their identical twins did not. Why the difference? The twins had the same genes. They ate the same food. They lived in the same village. But their gut microbes were very different.

These microbial communities change over time, much like plants colonising a burnt forest or a new island. Lichens and mosses come first, before giving way to shrubs, then trees. Likewise, in the gut, milk-eating microbes give way those that digest plant matter. Waves of species succeed and replace each other, until they settle on a stable, mature, and more diverse community. In a normal gut, this takes about three years. But in the kwashiorkor kids, the changing communities had stagnated, leaving them with immature microbes for their age.

When Gordon’s team transplanted these immature communities into mice with no microbes of their own, the rodents lost weight—but only if they also ate the equivalent of a poor Malawian diet. The combination of poor food and immature microbes triggered the symptoms of kwashiorkor.

But which microbes are important? Is it the entire community, with its hundreds or thousands of species? Or does the problem lie with a smaller cabal? To find out, Gordon relied on an antibody called IgA. Immune cells release this substance into the gut, where it piles onto microbes to create immobilising coats. Around half the bacteria in our gut are restrained in this way. By looking for these targeted species, “you can use the immune system to mine the microbiota,” says Gordon.

His postdocs Andrew Kau and Joseph Planer began by transplanting microbes from a pair of 21-month-old Malawian twins—one with kwashiorkor and one without—into germ-free mice. They then used a technique called BugFACS to pull out any bacteria that were restrained by IgA. They effectively used the antibody as a fishing rod to hook microbes that draw the immune system’s attention.

In the mice colonised by the ‘kwashiorkor’ microbes, IgA pulled out large numbers of Enterobacteriaceae (prounounced En-ter-oh-back-tee-ree-ay-see-ay). The team then loaded this IgA-targeted set of microbes into more germ-free mice. The rodents fared badly. Half of them died within five days. When the team looked at their guts under a microscope, they saw carnage.

A normal gut has tightly packed cells to prevent microbes from slipping through, and dense forests of tall pillars for absorbing nutrients. In these guts, the cells were pulling away from each other, and the pillars were shrunken and shredded. Imagine a fence with wide gaps between rotting slats. “The [lining] was really just torn apart,” says Gordon. “It was pervasive and dramatic.”

Kau and Planer isolated several of the bacteria within this lethal community and identified a set of 11 species that collectively destroy the gut. These included three Enterobacteriaceae, and several common gut inhabitants like Bacteroides fragilis and Bacteroides thetaiotamicron. Individually, these microbes did very little. Collectively, they led to shredded guts and severe weight loss. “It’s not just one actor,” says Gordon. “It’s the concentred effort of several organisms.”

And as before, the team showed that this cabal only harmed mice that ate a Malawian diet. If the rodents ate more nutritious meals, the microbes were benign. As the team showed in their earlier work, it’s the combination of diet and microbes that makes for poor health.

The team used the same techniques to show that healthy twins, who don’t get kwashiorkor, have guts that are rich in two particular bacteria. The first of these, Akkermansia muciniphila, can protect mice from being obese; it seems that it protects them from malnutrition too. The second one, Clostridium scindens, is part of a group that stops the immune system from overreacting. It was recently shown to single-handedly block infections by its deadlier cousin—Clostridium difficile, a bug that causes severe diarrhoea. These two microbes were enough to defend mice from the more destructive ones.

Having done all these experiments in mice, the team then returned to humans. They used their BugFACS technique on 19 more pairs of Malawian twins, to pull out the IgA-targeted microbes in their guts. And they found the same patterns: more Enterobacteriaceae meant a greater risk of kwashiorkor.

“This is a major advance in the field,” says Charlotte Kaetzel from the University of Kentucky, who studies IgA. “Of course, Jeff Gordon’s lab brings the most state-of-the-art methods to this type of study.” It’s important, she says, that the team combined experiments in germ-free mice, where microbes can be precisely controlled, with direct analyses of the stools of healthy and undernourished children.

This kind of approach is a staple of Gordon’s group. It lends weight to their claims that the microbes are actually causing kwashiorkor, rather than just going along for the ride, and that the patterns in mice are relevant to humans.

The team are now trying to understand how the 11 microbes that they identified damage the gut, and how C.scindens and A.muciniphila thwart them. They also want to know if the same patterns apply to malnourished people from other parts of the world, with different genes, diets, and cultural practices. In the long-term, they hope to develop ways of analysing a child’s microbes (perhaps, using BugFACS) to diagnose their risk of malnutrition before symptoms show, or even to develop probiotics containing bacteria that can forestall these diseases in places where food is scarce.

PS: I’ve written two pieces today about the microbiome. In this one, Akkermansia protected mice from malnutrition caused by other microbes and a poor diet. In the other, Akkermansia was associated with inflammatory disease, in mice that ate a diet rich in food additives. In other rodent studies, it stops mice from getting fat, but is more common in cases of bowel cancer. All of this illustrates a point I’ve made before: any one microbe can have very different effects in different contexts and circumstances. There is no universally “good” bacterium, no universally “healthy” microbiome.

]]>http://phenomena.nationalgeographic.com/2015/02/25/fishing-for-the-microbes-behind-malnutrition/feed/0Food Additives Inflame Mouse Guts By Disturbing Microbeshttp://phenomena.nationalgeographic.com/2015/02/25/food-additives-inflame-mouse-guts-by-disturbing-microbes/
http://phenomena.nationalgeographic.com/2015/02/25/food-additives-inflame-mouse-guts-by-disturbing-microbes/#commentsWed, 25 Feb 2015 18:00:45 +0000http://phenomena.nationalgeographic.com/?p=167096If you walk down the aisles of any supermarket, you’ll see what dietary emulsifiers can accomplish. This common class of food additives binds water and oils together, preventing mixtures of the two from splitting. They stabilise ice-cream and other frozen desserts, mayonnaise, salad dressings, and virtually every kind of processed food. “Anything that sits in a package on a supermarket shelf, and can stay there for a while, probably has emulsifiers in it,” says Andrew Gewirtz from Georgia State University.

These additives may confer stability to food, but they can also bring discord to the gut—at least in mice. Gewirtz has found that two common emulsifiers—caboxymethylcellulose (CMC) and polysorbate-80 (P80)—can change the roll call of bacteria in a mouse’s gut. They also make the gut more porous, allowing microbes to slip through its walls and reach the immune cells and blood vessels on the other side. As a result, the mice developed severe inflammation. They also put on weight, and their blood sugar went up.

The team only looked at laboratory mice, so it’s not clear if emulsifiers have the same effects in humans at the doses we normally eat (more on this later). Still, “this work cannot be ignored,” says Fergus Shanahan from University College Cork, who was not involved in the study. He doubts that most people would be significantly affected by occasionally eating foods with emulsifiers. But the calculus of risk might change for those who have a genetic predisposition to inflammatory bowel disease (IBD), or who eat lots of processed foods.

“The other implication is that current methods for testing food additives for safety are not adequate,” says Gewirtz. CMC and P80 are both “generally regarded as safe”, since they’re not toxic at the levels found in food, and they don’t cause cancer. But such tests say nothing about their ability to disturb the relationship between us and the microbes we carry—disturbances that have been linked to obesity, IBD, and other conditions.

The immunostat

Your immune system needs to spot and thwart infectious microbes, while maintaining a truce with trillions that live in your body and carry out important tasks. If it’s too twitchy, it will constantly go berserk whenever it notices our microbial companions and trigger chronic inflammation. If it’s too relaxed, it wouldn’t detect dangerous threats. It must react without overreacting.

It achieves this balance through a bewilderingly complex network of cells and molecules that I’m going to boil down into a single image. Think of the thermostat that stabilises the temperature of your room. Now picture an “immunostat” that, in a similar way, dictates how responsive the immune system is. Set it too low and you become vulnerable to infections; too high, and your run the risk of inflammatory diseases.

Many things affect where the immunostat is set, including genes, diet, infections, and more. Your gut microbes are also involved. Some groups provoke the parts of the immune system that exacerbate inflammation. Others stimulate the pacifying components that calm everything down. Physical barriers are also important. The simplest way of stopping the immune system from overreacting to microbes is to keep them separate. Our gut achieves this by keeping its cells tightly fused and covering them with a thick layer of mucus. Microbes sit on one side of this Great Wall of Mucus; immune cells on the other.

The experiments

Gewirtz suspects that emulsifiers disrupt both the mucus and the microbe communities, pushing the immunostat towards a twitchier setting.

His postdoc Benoit Chassaing fed lab mice with either CMC or P80, by adding both substances to their food or water at one part per hundred. When he looked at their guts under a microscope, he saw that their mucus wall was thinner than usual, and bacteria had penetrated deep into what was once a No Microbe’s Land. Some were actually touching the gut itself. The gut had also become leakier, so many microbes found their way through to the immune cells and blood vessels on the other side.

The emulsifiers also changed the communities of microbes within the rodents’ guts. Chassaing saw a rise in species that excel at triggering inflammation, and in those that eat mucus like Ruminococcus and Akkermansia. Other microbes shrank away, including groups that produce anti-inflammatory substances by digesting dietary fibre.

These changes lead to a vicious cycle of even more inflammation, even leakier guts, and even thinner mucus. The result: low-grade inflammation in normal lab mice, and a more severe form—colitis—in mutant rodents that were genetically susceptible to IBD.

After swallowing the emulsifiers, both breeds of rodents ate more food. They put on body fat and gained 10 grams in weight (on top of their normal 140). Their blood sugar levels went up. They became less sensitive to the hormone insulin. In other words, they showed many symptoms of metabolic syndrome—a condition that increase the risk of diabetes and heart disease.

Do the microbes cause these problems, or are they just along for the ride? It’s probably the former. None of these changes—the thinner mucus, the inflammation, or the metabolic problems—happened to germ-free mice that were raised in sterile conditions. Without their microbes, those rodents ate emulsifiers to no effect. But when Chassaing loaded them with microbes from individuals that had eaten emulsifiers, they too developed all the same symptoms. Whatever the additives are doing, they’re doing it via gut microbes.

The implications

Inflammatory bowel disease was once very rare, but has become more common since World War II. Many things that change our relationship with our microbes could have contributed to that rise, including antibiotics, sanitation, and dietary shifts, including an abundance of fat, a lack of fibre, or the presence of artificial sweeteners.

What about emulsifiers? It’s hard to say. To state the obvious, mice aren’t people. “Many observations in mice tell us a lot about host-microbe interactions but either don’t translate to humans or have far less significance in humans,” adds Shanahan. “The microbiota of a lab mouse is very simple and much simpler than that of humans. It doesn’t take much to significantly disturb it.” Many things can, including drugs like aspirin, antibiotics, other bacteria, and more. To Shanahan, it’s not surprising that dietary emulsifiers join the list. “What is surprising is that this would occur at such low levels, including levels that humans may be exposed to,” he adds.

But that’s another limitation: it’s hard to compare the doses that Chassaing used to the levels of emulsifiers we eat, because no good measurements of those levels exist. According to one report from the Food Safety Commission of Japan said, “In Western countries, the daily intake of polysorbates, based on their usage in food, was estimated at 12-111 milligrams per person per day.” That’s proportionally much less than what Chassaing’s rodents ate, but we have no idea if the Japanese estimates are reliable—the report provides no data or sources for its figures.

In the absence of such data, the team used the limits set by the US Food and Drug Adminstration, which approves the use of P80 at up to 1 percent in foods, and CMC at up to 2 percent. Chassaing used 1 percent levels in his experiments, but he also found signs of inflammation at 0.1 percent. “We gave amounts that approximate the total consumption of a person who eats a lot of processed food,” says Gewirtz. “It’s the best we could do at this time, but we need better estimates.”

“I went over the data, and they did a thorough job,”says Eugene Chang from the University of Chicago Medical Centre, who studied IBD. “There’s also precedent for this.” He points to other studies showing that carrageenan—another common emulsifier, derived from seaweed—can cause inflammatory bowel disease in mice.

Then again, there’s also some conflicting evidence from other animal studies—none of them have looked at microbes but a few have measured body weight. A Dutch team showed that CMC doesn’t affect the body weight of broiler chickens, and the US National Toxicology Program found that P80 doesn’t change the body weight of rats. Meanwhile, a Japanese study found that pregnant rats actually lost weight when given P80.

The FDA certainly isn’t changing its position. In a statement, it said, “The FDA closely monitors the scientific literature for information that might indicate a potential public health concern with a food substance. At this time, the FDA does not have sufficient evidence to alter its previous conclusion that polysorbate 80 and carboxymethyl cellulose are considered safe under their intended conditions of use in food.”

Meanwhile, Gewirtz says, “We’re certainly eating less processed food since we’ve been doing this work. It took a lot of effort, but we did find one type of ice-cream in the supermarket that’s emulsifier-free.”

]]>http://phenomena.nationalgeographic.com/2015/02/25/food-additives-inflame-mouse-guts-by-disturbing-microbes/feed/1G M CC BY 2.0]]>I’ve Got Your Missing Links Right Here (21 February 2015)http://phenomena.nationalgeographic.com/2015/02/21/ive-got-your-missing-links-right-here-21-february-2015/
http://phenomena.nationalgeographic.com/2015/02/21/ive-got-your-missing-links-right-here-21-february-2015/#commentsSat, 21 Feb 2015 20:02:02 +0000http://phenomena.nationalgeographic.com/?p=167080Sign up for The Ed’s Up—a weekly newsletter of my writing plus some of the best stuff from around the Internet.

Top picks

“Above all, I have been a sentient being, a thinking animal, on this beautiful planet, and that in itself has been an enormous privilege and adventure.” Oliver Sacks has terminal cancer and is going out in a blaze of poetry and beauty.

This video on epigenetics, as explained through Beethoven’s 5th, is a masterpiece of explanatory science communication, from Kerri Smith.

“The endangered dead“: a great feature on the threats facing natural history museums. By Christopher Kemp

The gorgeous typeface that drove men mad and spurred a 100-year mystery. By Kelsey Campbell-Dollaghan

“Why do you want to talk about this embarrassing corpse?” Tom Bartlett on the brutal response to the Human Brain Project.

]]>http://phenomena.nationalgeographic.com/2015/02/21/ive-got-your-missing-links-right-here-21-february-2015/feed/1Fast-Evolving Human DNA Leads to Bigger-Brained Micehttp://phenomena.nationalgeographic.com/2015/02/19/fast-evolving-human-dna-leads-to-bigger-brained-mice/
http://phenomena.nationalgeographic.com/2015/02/19/fast-evolving-human-dna-leads-to-bigger-brained-mice/#commentsThu, 19 Feb 2015 17:00:00 +0000http://phenomena.nationalgeographic.com/?p=167040Between 5 and 7 million years of evolution separate us humans from our closest relatives—chimpanzees. During that time, our bodies have diverged to an obvious degree, as have our mental skills. We have created spoken language, writing, mathematics, and advanced technology—including machines that can sequence our genomes. Those machines reveal that the genetic differences that separate us and chimps are subtler: we share between 96 and 99 percent of our DNA.

Some parts of our genome have evolved at particularly high speed, quickly accumulating mutations that distinguish them from their counterparts in chimps. You can find these regions by comparing different mammals and searching for stretches of DNA that are always the same, except in humans. Scientists started identifying these “human-accelerated regions” or HARs about a decadeago. Many turned out to be enhancers—sequences that are not part of genes but that control the activity of genes, telling them when and where to deploy. They’re more like coaches than players.

It’s tempting to think these fast-evolving enhancers, by deploying our genes in new formations, drove the evolution of our most distinguishing traits, like our opposable thumbs or our exceptionally large brains. There’s some evidence for this. One HAR controls the activity of genes in the part of the hand that gives rise to the thumb. Many others are found near genes involved in brain development, and at least two are active in the growing brain. So far, so compelling—but what are these sequences actually doing?

To find out, J. Lomax Boyd from Duke University searched a list of HARs for those that are probably enhancers. One jumped out—HARE5. It had been identified but never properly studied, and it seemed to control the activity of genes involved in brain development. The human version differs from the chimp version by just 16 DNA ‘letters’. But those 16 changes, it turned out, make a lot of difference.

Boyd’s team introduced the human and chimp versions of HARE5 into two separate groups of mice. They also put these enhancers in charge of a gene that makes a blue chemical. As the team watched the embryos of their mice, they would see different body parts turning blue. Those were the bits where HARE5 was active—the areas where the enhancer was enhancing.

Embryonic mice start building their brains on their ninth day of life, and HARE5 becomes active shortly after. The team saw that the human version is more strongly active than the chimp one, over a larger swath of the brain, and from a slightly earlier start.

HARE5 seems to be particularly active in stem cells that produce neurons in the brain. The human version of the enhancer makes these stem cells divide faster—they take just 9 hours to split in two, compared to the usual 12. So in a given amount of time, the mice with human HARE5 developed more neural stem cells than those with the chimp version. As such, they accumulated more neurons.

And they developed bigger brains. On average, their brains were 12 percent bigger than those of their counterparts. “We weren’t expecting to get anything that dramatic,” says Debra Silver, who led the study.

“Ours stands as among the first studies to demonstrate any functional impact of one of these HARs,” she adds. “It shows that just having a few changes to our DNA can have a big impact on how the brain is built. We’ve only tested this in a mouse so we can’t say if it’s relevant to humans, but there’s strong evidence for a connection.”

“I’m really excited that people are following up [on these HARs] and finding out what they do,” says Katherine Pollard from the Gladstones Institutes, who was one of the scientists who first identified these sequences. “It’s been really daunting to figure out what the heck these things do. Each one takes years. These guys went the extra mile beyond what everyone else has been doing, by showing changes in the cell cycle and in brain size.”

“It’s a very clever use of mice as readouts for human-chimp differences,” says Arnold Kriegstein from the University of California, San Francisco. “The [brain] size difference isn’t terribly big, but it’s certainly in the correct direction.”

Eddy Rubin from the Joint Genome Institute is less convinced. His concern is that the team’s methods could have saddled the mice with multiple copies of HARE5 in various parts of their genome. As such, it’s not clear if the differences between the two groups are due to these factors, rather than to the 16 sequence differences between the human and chimp enhancers. “[That] casts major shadow on the conclusions,” says Rubin. “This is an interesting study pursuing an important issue, but the results should be taken with a grain of salt.”

Regardless, Silver’s team are now continuing to study HARE5. Now that their mice have grown up, they are designing tests to see if the adults behave differently thanks to their larger brains. This is important—bigger brains don’t necessarily mean smarter animals. They’re also looking into a few other enhancers. One of them, for example, seems to a control a gene that affects the growth of neurons.

“I think HARE5 is just the tip of the iceberg,” says Silver. “It is probably one of many regions that explain why our brains are bigger than those of chimps. Now that we have an experimental paradigm in place, we can start asking about these other enhancers.”

]]>http://phenomena.nationalgeographic.com/2015/02/19/fast-evolving-human-dna-leads-to-bigger-brained-mice/feed/14Why Do Luna Moths Have Such Absurdly Long Tails?http://phenomena.nationalgeographic.com/2015/02/16/why-do-luna-moths-have-such-absurdly-long-tails/
http://phenomena.nationalgeographic.com/2015/02/16/why-do-luna-moths-have-such-absurdly-long-tails/#commentsMon, 16 Feb 2015 20:00:53 +0000http://phenomena.nationalgeographic.com/?p=167025You don’t need a field guide to recognise a luna moth. This large insect, found throughout the eastern half of North America, is unmistakeable. It has a fuzzy white body, red legs, feathery yellow antennae, and huge lime-green wings that can stretch up to 4.5 inches across. And at the end of its hindwings are a pair of long, streaming tails that can double the moth’s length.

In 1903, an entomologist named Archibald Weeks suggested that the tails direct predators away from the moth’s body. “Again and again may predator bat or bird, in an effort to capture a moth or butterfly, successively tear away sections of the tails, of which a sacrifice can be readily afforded, without disabling it or retarding its flight,” he wrote.

He was roughly right. More than a century on, Jesse Barber from Boise State University has shown that the luna moth’s tails are the equivalent of eyespots on fish and butterflies. These distinctive markings are typically found on dispensable body parts like tails and outer wings. They serve to draw a predator’s attention away from more vulnerable regions; better to lose a tail than a head.

Eyespots are visual defences, and bats—the main nemeses of moths—are not visual hunters. They find their prey with sonar—they make high-pitched squeaks and visualise the world using the rebounding echoes. To divert a bat, you need something that makes distracting echoes.

That, according to Barber, is what the luna moth’s tails do. They are “auditory deflectors”. Bat distractors.

Barber pitted luna moths against bats in a dark room, and filmed their encounters with infrared cameras. Under normal circumstances, the bats only managed to snag 35 percent of the moths. But if Barber cut off the insects’ tails beforehand, the bats caught 81 percent of them. That’s not because they become worse fliers—in fact, the tails don’t seem to affect their aerial abilities at all.

When bats aim their sonar at insects, they analyse the rebounding echoes for the distinctive signatures of beating wings. But the luna moths tails, which spin behind them as they fly, also produce echoes that resemble wingbeats. To the bat, they either sound like a very conspicuous part of their target, or like a different target entirely. As a result, they fumble their attacks.

When bats attack, they usually use their wings and tail to scoop an insect towards their faces, so they can deliver a killing bite to their victim’s body. But when bats attack luna moths, they aim about half their attacks at the tails. That’s a mistake—only 4 percent of those attacks succeed. Sometimes, the bat misses the moth entirely (see above). Other times, it bites off a tail while the moth escapes—down one inessential body part, and still alive (see below).

The tails also make the luna moths bigger, which might make them harder for the bats to handle and dispatch. But when Barber pitted bats against the polyphemus moth—an even bigger species that lacks tails—he saw that the predators killed 66 percent of their targets. The luna moths, despite being smaller, were harder to catch. “Clearly, tails provide an anti-bat advantage beyond increased size alone,” Barber wrote.

It’s possible that female moths also judge the health and quality of a male by looking at the size of his tails. But this doesn’t fit with the moths’ behaviour. Female moths spend most of their time hiding in protected nests and drawing males to them by releasing pheromones. They also mate with the first males they find, so there’s no evidence that they’re choosy—much less that they choose on the basis of tail length.

Luna moths belong to a group of large moths called the saturniids—a group that contains members like Copiopteryxand Eudaimonia, with even more extreme tails. By comparing the tail lengths of 113 saturniid species, Barber showed that these moths have evolved long tails on at least four separate occasions. He now wants to know if these other species are also good at foiling bats.

]]>http://phenomena.nationalgeographic.com/2015/02/16/why-do-luna-moths-have-such-absurdly-long-tails/feed/3I’ve Got Your Missing Links Right Here (14 February 2015)http://phenomena.nationalgeographic.com/2015/02/14/ive-got-your-missing-links-right-here-14-february-2015/
http://phenomena.nationalgeographic.com/2015/02/14/ive-got-your-missing-links-right-here-14-february-2015/#commentsSat, 14 Feb 2015 17:00:41 +0000http://phenomena.nationalgeographic.com/?p=167009Sign up for The Ed’s Up—a weekly newsletter of my writing plus some of the best stuff from around the Internet.

]]>http://phenomena.nationalgeographic.com/2015/02/14/ive-got-your-missing-links-right-here-14-february-2015/feed/0There’s No Plague on the NYC Subway. No Platypuses Either.http://phenomena.nationalgeographic.com/2015/02/10/theres-no-plague-on-the-nyc-subway-no-platypuses-either/
http://phenomena.nationalgeographic.com/2015/02/10/theres-no-plague-on-the-nyc-subway-no-platypuses-either/#commentsTue, 10 Feb 2015 21:30:35 +0000http://phenomena.nationalgeographic.com/?p=166990There is no good evidence that Yersinia pestis—the bacterium that causes plague—is riding aboard the New York City subway. That’s the message from several microbiologists, in response to a wave of news stories that emerged last Friday.

“Plague, anthrax and cheese? Scientists map bacteria on New York subway,” said the Guardian. “From beetles to bubonic plague: Bizarre DNA found in NYC subway stations,” proclaimed the Washington Post. “Terrifying microbe map of New York’s subway system reveals superbugs, anthrax and bubonic plague,” blathered the Daily Mail, duly retaining its crown as the champions of scaremongering.

All of these stories were based on a census of some of New York City’s smallest residents—its microbes. Over the course of 18 months, a team of scientists led by Christopher Mason from Weill Cornell Medical College swabbed surfaces all over the city, including every open subway station (see a video about their subway sampling here). They then analysed the DNA in their samples to identify the microbes that lived on each surface.

There were plenty of interesting results. For example, the bacteria from South Ferry Station, which was flooded by Hurricane Sandy in 2012, were closer to marine microbes than to those in the rest of the subway. But the team’s most notable claims were that they found DNA from the plague bacterium Yersiniapestis in three samples, and from the anthrax bacterium Bacillus anthracis in two. These nuggets predictably wound their way into every major news story.

The researchers downplayed the significance of these results, saying that if Y.pestis was present, it was unlikely to be “active and causing disease in people”. As Mason told the New York Times, “We’re saying there’s evidence for these things… but no one should worry.”

But several microbiologists think that even this statement goes too far. “[They] have not provided persuasive evidence that the agents that cause plague or anthrax are present anywhere in the New York City subway system,” says Ian Lipkin, a well-respected virus hunter from Columbia University. “The genetic footprints they report are not specific for the agents that cause anthrax or plague; they are also found in other common bacteria that are not associated with disease.”

The team arrived at their conclusions after compiling the DNA in each sample, breaking it down into smaller pieces, and then sequencing the fragments. They then searched for these sequences—or “reads”—in a public database of genes from all known organisms. If they found many matches for a given microbe, they concluded that said microbe was present in their samples.

“This method is notoriously unreliable,” says Willem van Schaik from Utrecht University, who studies antibiotic-resistant bacteria. As Lipkin also noted, it’s prone to false alarms, because a given read could match DNA that’s found in many other bacteria besides Y.pestis.

Rob Knight, formerly at the University of Colorado Boulder, showed just how ludicrous this problem can get last year. His colleague, Andrea Ottesen at the FDA, swabbed tomato plants in a field in Virginia, and Knight analysed the DNA in those samples. He found matches to the duck-billed platypus—an Australian animal, not known to live in Virginia. They then analysed over 19,000 publicly available microbiome samples from around the world; around a third threw up matches for platypus DNA. Either the platypus secretly rules the world or, more likely, this was a hilarious case of false positives gone mad. The team even created a programme called Platypus Conquistador to rectify the problem.

There are signs of similar problems in the subway paper. In the case of Y.pestis, the team found several reads that matched a plasmid—a free-floating ring of DNA that sits outside the bacterium’s main genome. They highlighted one particular section of the plasmid in one of their figures. Based on this, Van Schaik did his own search and found that sequences in this section are also found in at least three other bacterial species.

Mason’s team also identified DNA from many eukaryotes—that’s animals, plants, and other complex organisms—and listed the top species in one of their tables. They were, starting from the top: the mountain pine beetle, which lives in the west coast of North America; the Mediterranean fruit fly, which does not exist in the continental US; the cucumber; and humans. Hmm. The fly, in particular, is a major agricultural pest and the subject of intensive surveillance. Its presence in New York is “so unlikely that I think the approach they used is just flawed,” says Van Schaik.

Unlike the fly, Y.pestisdoes exist in the US, but in the southwest where it infects rodents. It is a stranger to New York. Lipkin’s team have done extensive surveys of the city’s rats and failed to find Y.pestis in any of them.

To convince their critics, Mason’s team would have to show that reads from the subway analysis map to the entirety of the Y.pestis plasmid. Then again, plasmids can easily move from one bacterium to another, so it would be even more convincing to show reads that map to Y.pestis’s actual chromosome. “Even better would be to prove the existence of Y. pestis through some independent means, such as culture,” says Nick Loman from the University of Birmingham, who studies the genomes of disease-causing microbes. By “culture”, he means trying to actually grow bacteria from collected samples.

I contacted Chris Mason about these criticisms and he is preparing a blog post to address them, and others that he has received. [Update 18 Feb: Mason has published the post and it is humble, informative, detailed, and introspective]

As I mentioned, the paper has other interesting results and it might seem churlish to pick on this one. But it symbolises some of the problems in the study of microbiomes—the collections of bacteria that live in specific animals or environments. Microbiome research is among the hottest fields in biology and is attracting hordes of enthusiastic scientists. This is great—(disclosure: I’m writing a book on animal microbiomes)—but the field also risks throwing up a lot of misleading and false conclusions if methods aren’t applied properly and results aren’t analysed cautiously. (Last November, I wrote about another common problem that might lead to false positives in a lot of microbiome studies.)

One could argue that these issues come out in the wash, and that science corrects itself. Indeed, Mason told the New York Times that not reporting the fragments of anthrax and plague “would have been irresponsible”. Then again, readers were hit with a wave of headlines that raised the possibility of plague on the subway. “If I wasn’t a microbiologist, I would be scared by this and rightfully so,” says Van Schaik.

Marc Lipsitch, an epidemiologist from the Harvard School of Public Health, agrees, and adds that panic-quelling follow-up stories, like this one, don’t help matters. “Stories that present a highly hedged finding as news, but then say “Don’t worry”, make scientists seem like we aren’t telling the whole truth,” he says. “Either it is news, or we shouldn’t worry, but it’s tough to see how both could be true.”

Update: Nick Loman has put up a short post illustrating one of the problems I talked about in this post. He took E.coli, shred its DNA, sequenced the pieces, and then matched them up to databases. By right, 100% of the reads should come out as E.coli. In fact, just 61% of them did.

Correction: The article was amended to note that Andrea Ottesen swabbed the tomato plants, rather than Rob Knight himself.

]]>http://phenomena.nationalgeographic.com/2015/02/10/theres-no-plague-on-the-nyc-subway-no-platypuses-either/feed/4Marc A. Hermann , CC BY 2.0]]>I’ve Got your Missing Links Right Here (07 February 2015)http://phenomena.nationalgeographic.com/2015/02/07/ive-got-your-missing-links-right-here-07-february-2015/
http://phenomena.nationalgeographic.com/2015/02/07/ive-got-your-missing-links-right-here-07-february-2015/#commentsSat, 07 Feb 2015 17:00:48 +0000http://phenomena.nationalgeographic.com/?p=166977Sign up for The Ed’s Up—a weekly newsletter of my writing plus some of the best stuff from around the Internet.

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I can. It’s a loud screeching noise in the background of our phone call.

“That’s a female rhesus freaking out,” he says.

Rhesus macaques have featured heavily in lab experiments, but this particular loud female is part of a wild group, living in Puerto Rico. Higham, an anthropologist from New York University, is studying them. He is interested in their faces, which vary from a dull pink to a vivid red. Specifically, he wants to know if the females judge the males on the intensity of that colour.

“I’m stood about 5 metres away from a sub-adult male and he’s with a 3-year-old female, and they’ve been mating a lot,” he says. “There are lots of other monkeys here, and the big, blue Caribbean sea around me.” As field work goes, it’s not hard.

The same couldn’t be said for the other group of funky-faced monkeys that Higham has been studying—the guenons. These African monkeys are known for their beautiful and diverse faces. De Brazza’s monkey has a white moustache and beard, and an orange sun rising on its forehead. The crowned guenon: dark eyeshadow, a black quiff, a pair of white forehead highlights, and a luxurious golden beard. The red-eared guenon: a drunk’s pink nose, a black brow ridge, white tufts around its eyes, and—yes—red ears. Every species of guenon, and there are between 24 and 36 of them, has its own distinctive facial marks.

Why?

In the 1980, zoologist James Kingdon suggested that they recognise members of their own species by their faces. Many of these monkeys live in the same place, and some travel in large mixed groups. They live, feed, and watch out for predators together, but when it comes time to mate, their faces help them to find partners of their own kind.

The idea made sense; testing it has been difficult. For a start, guenons live in forest canopies and move quickly. It’s hard to look at their faces, let alone look at them looking at each other’s faces.

Their patterns are also complicated, so how do you objectively compare them? If two guenons have yellow sideburns and pink noses, but differently shaped brows and differently coloured eyes, are they similar? A bit different? Very different? Humans are terrible at this kind of task; we have to limit ourselves to comparing specific features, which Kingdon found frustrating.

Higham opted for a different approach. He and postdoc William Allen took hundreds of photos of 22 guenon species in various zoos and wildlife sanctuaries, and analysed them with the eigenface technique—a facial recognition programme developed in the 1980s. It can quantify how distinctive two faces are by comparing them across many features simultaneously.

The technique revealed that guenon species have more distinctive faces when they live together. This supports Kingdon’s hypothesis that the colourful facial palettes help neighbouring monkeys to recognise their own kind, despite sharing the same forests. By contrast, if the faces were adaptations to something in the monkeys’ environment—say, light levels—then species that live together should look more similar. In fact, it’s the opposite.

Next, Higham and Allen wanted to know if the monkeys could glean any more information from each other’s faces. Could guenons tell each other’s age or gender? Could they recognise individuals, as we humans can?

The duo used a computer programme to analyse 541 images from the same photo set, on the basis of either overall patterns or specific features—like the brightness, colour, shape, or size of their eyebrows and nose spots. They wanted to see if the programme could, based on these traits, classify the monkeys by species, age or gender, or recognise individuals. For example, after seeing photos of different monkeys, could the programme accurately identify one in a new photo? Likewise, after seeing photos of monkeys of both genders, could it tell if a new monkey was male or female?

The programme flunked the age and gender tests—there’s apparently nothing in a guenon’s face that reveals either characteristic. But it excelled at both species and individual recognition. The former isn’t surprising but the latter is.

As Kingdon suggested and Higham confirmed, guenons have evolved to look as different as possible when they live together. The need for differences between species ought to constrain the differences within them. “If you start looking very different from others of your species, you run the risk of being mistaken for something else,” says Higham. This kind of “stabilising selection” should lead to distinctive species but lookalike individuals—and yet that’s not what he found. One guenon can potentially tell its neighbours apart with a glance.

Of course, there’s no guarantee that what the programme is seeing is what the guenons actually see. Higham is now carrying out some experiments to see if the differences that the computer can glean are actually obvious to the monkeys themselves. He has even played around with drones to see if he can get a closer view of the guenons as they clamber through the canopy.

In the meantime, he thinks that his methods will be broadly useful to scientists who study animal signals. “There’s a lot of work on colour signals in animals and a lot of it is quite simple, like: This lizard patch varies from pale pink to bright pink,” he says. “But a lot of these signals are very complex. So, how do you measure them?” Computer learning offers an option. “That’s true whether it’s a guenon or a paper wasp or a paradise flycatcher or anything really.”